Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion.

Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Research Abstract Details 

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Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Abstract Text:

Shayne F Andrew,Thu T Dinh,Sue Ritter,

Glucose is required for brain energy metabolism. Decerebration, aqueduct occlusion, and cannula mapping studies have established that glucose-sensing cells capable of eliciting feeding and adrenal medullary responses to glucoprivation are localized in the hindbrain. Glucoprivation also evokes corticosterone and glucagon secretion, but the location of receptors mediating these responses is unknown. To determine whether glucoreceptive sites controlling these responses are present in the hindbrain, we administered the antiglycolytic agent, 5-d-thioglucose (5TG, 24 microg in 200 nl) into brain stem sites through implanted cannulas and examined plasma concentrations of corticosterone and glucagon. Both hindbrain and hypothalamic sites were tested. Blood was collected remotely from intra-atrial catheters at 0, 30, 60, 90, 120, 180, and 240 min after 5TG or control injection. Caudal hindbrain 5TG injections potently increased circulating corticosterone and glucagon concentrations. For corticosterone, the mean peak response (maximum concentration minus time 0 concentration) elicited at positive sites (23 of 40 sites) was 391 ng/ml (SE = 16). For glucagon, the mean peak response at positive sites (27 of 40 sites) was 46 pg/ml (SE = 6). Glucoprivically evoked glucagon secretion was abolished by the ganglionic blocker, hexamethonium, but not by adrenal denervation. Six of twenty-five hypothalamic sites were positive for corticosterone secretion, yielding plasma levels of 279 +/- 23 ng/ml, but none of the hypothalamic injection sites elevated glucagon concentrations. Results demonstrate that receptor cells responsive to glucose deficit and capable of increasing corticosterone and glucagon concentrations exist within the hindbrain, thus further delineating central glucoregulatory neural circuitry.

Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Publishing Authors By Initials

SF Andrew,TT Dinh,S Ritter,

For similar natural sciences: time: time factors research abstracts see: natural sciences: time: time factors research

PUBMED ID PMID:

MEDLINE DATE:

Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Regulatory, integr

VOLUME: 292

Page Numbers: R1792-8

Journal Abbreviation:

ISSN: 0363-6119

DAY: 11

MONTH: 01

YEAR: 2007

Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901230

Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Keywords Mesh Terms:

KEYWORDS: Time Factors

MESH TERMS: metabolism

Chemical & Substance for Abstract: Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion. Information

Substance Name: Glucagon

Registry Number: 9007-92-5

Grant and Affiliation Information for Localized glucoprivation of hindbrain sites elicits corticosterone and glucagon secretion.

AFFILIATION: Programs in Neuroscience, Washington State Univ, Pullman, WA 99164-6520, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS045520

ACRONYM: NS

MEDLINETA: Am J Physiol Regul Integr Comp

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